Chapter 48 - Somatic Sensations: General Organization, Tactile and Position Senses

• Mechanoreceptors (touch, pressure, vibration)
• Thermoreceptors (cold, warmth)
• Nociceptors (pain/tissue damage)
• Electromagnetic receptors (light, in the retina)
• Chemoreceptors (taste, smell, blood gases, osmolality)

• Rapidly adapting (phasic) receptors - Pacinian corpuscles, hair follicle receptors. Respond only during change, not sustained pressure. Adaptation occurs via structural fluid redistribution and Na+ channel inactivation.
• Slowly adapting (tonic) receptors - Merkel's discs, Ruffini endings, muscle spindles, baroreceptors, pain receptors. Maintain firing throughout sustained stimuli.

• Organized as a sensory homunculus - body mapped across cortex
• Hands, lips, and tongue have disproportionately large representation (highest receptor density)
• Area 3a: muscle spindle signals; Area 3b: slowly adapting cutaneous touch; Area 1: rapidly adapting cutaneous touch; Area 2: deep pressure and joint position

Chapter 49 - Somatic Sensations: Pain, Headache, and Thermal Sensations

• Fast (sharp) pain: Aδ fibers, onset in ~0.1 second, well-localized, sharp/pricking quality
• Slow (burning/aching) pain: C fibers, onset after 1+ second, poorly localized, associated with tissue destruction and emotional suffering

• Free nerve endings in skin, periosteum, joint surfaces, arterial walls, meninges
• Notably absent in brain parenchyma
• Activated by: mechanical damage, temperatures >45°C, and chemical mediators (bradykinin, serotonin, histamine, K+ ions, acids, substance P)
• Critically, they do not adapt - sustained damage causes sustained pain

1. Neospinothalamic tract (fast pain): Aδ fibers → laminae I, V of dorsal horn → decussate → ascend in anterolateral column → VPL thalamus → somatosensory cortex. Provides precise spatial localization.
2. Paleospinothalamic tract (slow pain): C fibers → laminae II (substantia gelatinosa), III, V → decussate → ascend → periaqueductal gray (PAG), reticular formation, intralaminar thalamic nuclei → limbic system. Responsible for suffering, emotional response, poor localization.

• Intracranial: from meninges, dural sinuses, vessels (brain parenchyma is insensitive)
• Migraine: vasoconstriction (aura) followed by vasodilation + neurogenic inflammation; involves serotonin dysregulation
• Tension headache: sustained scalp/neck muscle contraction causing local ischemia
• Cluster headache: episodic, unilateral periorbital, with autonomic features (lacrimation, ptosis)

• Cold: Aδ fibers, peak sensitivity ~25°C
• Warm: C fibers, peak sensitivity ~38°C
• Paradoxical cold: cold receptors fire at temperatures >45°C (why very hot stimuli feel "icy")
• Thermal signals travel with pain fibers in the anterolateral spinothalamic tract - less precise localization than touch

Chapter 55 - Spinal Cord Motor Functions; The Cord Reflexes

• Muscle spindles detect muscle length. Ia fibers (annulospiral endings on nuclear bag fibers) detect both rate of stretch and static length; Type II fibers (flower spray on nuclear chain fibers) detect static length only.
• The stretch reflex is the only monosynaptic reflex: stretch → Ia fires → directly excites alpha motor neuron → muscle contracts.
• Dynamic response: rate-sensitive, resists rapid length change
• Static response: maintains set muscle length
• Gamma motor neurons co-activate with alpha neurons to keep spindles sensitive during voluntary muscle contraction

• Located at muscle-tendon junction
• Detects tension (not length); Ib afferents → inhibitory interneurons → inhibit the same muscle
• Protective against excessive force; also excites antagonists

• Polysynaptic; noxious stimulus → pain afferents → flexor motor neurons excited → limb withdraws
• Multiple interneurons cause prolonged afterdischarge (reverberating circuits continue signaling after stimulus ends)

• Occurs 200-500 ms after a flexor reflex in the opposite limb
• Withdrawing one limb → contralateral limb extends to bear body weight
• Commissural interneurons cross the midline
• Shows the spinal cord coordinating bilateral limb movement

• Positive supporting reaction, cord righting reflexes
• Central pattern generators (CPGs): spinal circuits that produce rhythmic stepping movements without brain input - a spinal cat can walk on a treadmill

Chapter 56 - Cortical and Brain Stem Control of Motor Function

1. Primary Motor Cortex (MI, Area 4) - precentral gyrus
   • Contains giant Betz cells (the largest neurons in the CNS)
   • Somatotopically organized as the motor homunculus - hands and face dominate
   • Controls precise, discrete, voluntary movements - especially distal muscles (finger individuation)
   • Direct monosynaptic connections to spinal motor neurons for hand muscles
2. Premotor Area (PMA, Area 6)
   • Programs complex sequences of movement
   • Receives input from sensory cortices and association areas
   • Involved in visually guided movements and learned motor programs
3. Supplementary Motor Area (SMA)
   • Medial surface, superior to MI
   • Fires before movement begins, even during mental rehearsal
   • Critical for bilateral movements and internally generated sequences
   • Lesion: difficulty initiating voluntary movement

• ~1 million fibers from MI (30%), PMA/SMA (30%), somatosensory cortex (40%)
• Route: posterior limb of internal capsule → cerebral peduncles → medullary pyramids → pyramidal decussation (80-90% cross) → lateral corticospinal tract
• The remaining 10-20% descend ipsilaterally as the anterior corticospinal tract
• Key function: precise control of distal extremities, particularly individual finger movements

• Red nucleus → rubrospinal tract (distal limb control, works in parallel with corticospinal)
• Reticular formation → reticulospinal tracts (posture, axial/proximal muscles)
• Vestibular nuclei → vestibulospinal tracts (posture, anti-gravity tone)
• Basal ganglia → thalamus → feedback loop to cortex
• Pontile nuclei → cerebellum (via pontocerebellar fibers)

• Receives input from MI and from cerebellum (dentate nucleus via superior cerebellar peduncle)
• Rubrospinal tract decussates and descends in lateral funiculus
• Alternative/backup pathway for distal limb control when corticospinal tract is damaged

• Pontine (medial) reticulospinal tract: excites extensor tone
• Medullary (lateral) reticulospinal tract: inhibits extensors, facilitates flexors
• Controls posture and axial movements; modulated by cortex and cerebellum

• Utricle macula (horizontal plane): detects linear acceleration and static head tilt
• Saccule macula (vertical plane): detects vertical linear acceleration, head orientation when lying down
• Hair cell transduction: statoconia (CaCO3 crystals) bend stereocilia; bending toward kinocilium = depolarization = excitation; bending away = hyperpolarization = inhibition
• Semicircular canals: detect angular (rotational) acceleration in all three planes via endolymph movement
• Lateral vestibulospinal tract: strongly facilitates extensor (antigravity) muscles - essential for standing
• Medial vestibulospinal tract: controls neck muscles and vestibulo-ocular reflex

• Transection between superior and inferior colliculi → strong extensor spasm of all limbs
• Caused by loss of inhibitory cortical/red nucleus input with preservation of facilitatory vestibulospinal and pontine reticulospinal pathways
• Demonstrates that vestibular and reticular pathways dominate extensor tone when cortical inhibition is removed

• UMN lesion (Ch. 56 pathway damage): spasticity, hyperreflexia, Babinski sign, clasp-knife response - loss of cortical inhibition releases spinal cord circuits (Ch. 55)
• LMN lesion: flaccidity, hyporeflexia, fasciculations, muscle atrophy
• Referred pain patterns (Ch. 49): guide localization of visceral disease
• Gate control (Ch. 49) and transcutaneous nerve stimulation (TENS) are built on the same spinal cord synaptic architecture described in Ch. 55
• Spinal shock vs. decerebrate rigidity both illustrate the dependency of lower motor circuits on descending supraspinal tone